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Biomedical subjects

C A Carvalho

Publications and source records attributed to C A Carvalho.

At least 19 recordsLinked to original sources

Central serous chorioretinopathy after epidural corticosteroid injection.

PURPOSE: To report three patients who developed central serous chorioretinopathy after epidural corticosteroid injection for treatment of back pain. DESIGN: Interventional case series. METHODS: Three men, aged 73, 52, and 73 years, presented with bilateral central serous chorioretinopathy after corticosteroid injection in the epidural space for treatment of back pain. In all three cases, we did not initially elicit the history of corticosteroid use. RESULTS: Two of the three patients, aged 52 and 73 years, had diffuse retinal pigment epitheliopathy and one, aged 73 years, had classic central serous chorioretinopathy. Two patients had a spontaneous resolution of the subretinal fluid in both eyes. One patient had laser photocoagulation in both eyes but continued to have diffuse leakage in one eye. CONCLUSIONS: A careful history to determine corticosteroid use, including possible intrajoint and epidural injection, should be performed in older people with serous detachment of the macula, particularly when bilateral.

Aged↗

Pollen spectrum of honey of "uruçu" bee (Melipona scutellaris Latreille, 1811).

In spite of the importance of the "uruçu" bee as honey producer of excellent quality, as well, potential pollinator both in agricultural and natural ecosystems, mainly in North-eastern Brazil, just some information is found in literature about sources that such bees utilize to collect nectar and pollen. The identification of the plants visited by Melipona scutellaris was accomplished with base on the analysis of pollen types found in the honey samples collected every two months, from March 1997 to February 1998, in 15 colonies located in Catu, State of Bahia, Brazil (12 degrees 21'00"S, 38 degrees 22'40"W, 76 m of altitude). Qualitative and quantitative analysis of the pollen types were carried out determining the percentage and occurrence classes. Twenty-eight pollen types were found, being considered dominant pollen, the Eucalyptus spp. and Psidium sp. types and secondary pollen, Bauhinia sp., Caesalpinia sp. and Mimosa verrucata types. It was verified dominant pollen of Eucalyptus spp. in honeys produced in November/December 1997 and January/February 1998. The families Caesalpiniaceae (14%), Mimosaceae (25%) and Myrtaceae (56%) were the most represented in the pollen spectrum.

Animals↗

The effects of carotid endarterectomy on the retrobulbar circulation of patients with severe occlusive carotid artery disease. An investigation by color Doppler imaging.

OBJECTIVE: To analyze the effects of carotid endarterectomy on the retrobulbar circulation of patients with severe occlusive carotid artery disease (OCAD) by means of color Doppler imaging (CDI). DESIGN: Prospective. PARTICIPANTS: A total of 17 consecutive patients with severe OCAD and neurologic symptoms (with a history of transitory ischemic attack or cerebral vascular accident) participated. INTERVENTION: All 17 patients underwent carotid endarterectomy. The CDI of both orbits was performed by one masked investigator before surgery and at 1 week and 1 month after surgery. MAIN OUTCOME MEASURES: Peak systolic velocity, end diastolic velocity, and resistive index of the ophthalmic, central retinal, and temporal short posterior ciliary arteries were measured. The authors compared the hemodynamic parameters at all intervals. RESULTS: Peak systolic and end diastolic velocities in the ophthalmic, central retinal, and temporal short posterior ciliary arteries increased significantly 1 week and 1 month after carotid endarterectomy (P < 0.05). After surgery, the resistive indices in the central retinal and temporal short posterior ciliary arteries decreased significantly at both intervals (P < 0.05). The six patients who had reversed ophthalmic artery flow before surgery showed forward ophthalmic artery flow after carotid endarterectomy. The contralateral orbits showed no significant hemodynamic change after endarterectomy (P < 0.05). CONCLUSIONS: Hemodynamic changes in patients with severe OCAD undergoing carotid endarterectomy suggest improvement in the ipsilateral retrobulbar blood flow.

Aged↗

Collateral blood supply through the ophthalmic artery: a steal phenomenon analyzed by color Doppler imaging.

OBJECTIVE: This study aimed to evaluate the retrobulbar circulatory effects of reversed ophthalmic artery flow (ROAF) on the ophthalmic artery branches by means of color Doppler imaging. DESIGN: The design was a case-controlled study. PARTICIPANTS: Among 56 consecutive patients with severe (>70% stenosis) occlusive carotid artery disease, 15 patients (26.8%) with ROAF were identified. The control group consisted of 15 patients with similar degrees of carotid artery stenosis and forward ophthalmic artery flow. INTERVENTION: Arteriography and measurement of the retrobulbar hemodynamic parameters with color Doppler imaging were performed. MAIN OUTCOME MEASURES: Blood flow velocities and resistive index in the ophthalmic, central retinal, and temporal short posterior ciliary arteries were measured. RESULTS: Arteriography confirmed the diagnosis of ROAF in all 15 patients. There was no patient with ROAF diagnosed by arteriography and not diagnosed by color Doppler imaging. The frequency of bilateral severe occlusive carotid artery disease was significantly higher in the ROAF group (40%) compared to the control group (6.6%) (P = 0.04). Patients with ROAF showed significantly reduced vascular resistance in the ophthalmic artery (P = 0.03), higher vascular resistance, and lower blood flow velocities in the central retinal and temporal short posterior ciliary arteries (P < 0.05). CONCLUSION: This study suggests that patients with ROAF show a steal phenomenon, characterized by a shunt to the low-resistance intracranial circuit and reduction of retrobulbar blood flow.

Aged↗

Clinical findings and hemodynamic changes associated with severe occlusive carotid artery disease.

OBJECTIVE: The purpose of the study was to evaluate the ophthalmologic findings and to analyze the retrobulbar hemodynamics of patients with severe (greater than 70% stenosis) occlusive carotid artery disease (OCAD) by means of color Doppler imaging (CDI). DESIGN: A case-controlled study. PARTICIPANTS: Fifty-six consecutive patients with severe OCAD and an age- and sex-matched control group consisting of 56 healthy patients without OCAD were studied. INTERVENTION: All 112 patients underwent a complete ophthalmologic examination. Color Doppler imaging of both orbits was performed by one masked investigator. MAIN OUTCOME MEASURES: Peak systolic velocity, end diastolic velocity, and the resistive index of the ophthalmic, central retinal, and temporal short posterior ciliary arteries were measured. The authors compared the hemodynamic parameters measured in patients with severe OCAD with those obtained in the control group. The hemodynamic parameters of patients with asymmetric OCAD (stenosis > 70% in one internal carotid artery and stenosis < 50% in the contralateral artery) were also compared. In an attempt to determine risk factors associated with the ocular ischemic syndrome (OIS), the authors compared patients with severe OCAD and OIS with patients with severe OCAD without OIS. RESULTS: Peak systolic and end diastolic velocities in the ophthalmic, central retinal, and temporal short posterior ciliary arteries were significantly lower in patients with severe OCAD (P < 0.01). The mean resistive indices in the central retinal and temporal short posterior ciliary arteries were higher in the group with severe OCAD (P < 0.01). Similar results were obtained in the analysis of 25 patients with asymmetric carotid stenosis. Younger age (P = 0.012), severe bilateral OCAD (P = 0.01), high-grade carotid stenosis (P = 0.013), and reversed ophthalmic artery flow (P = 0.038) were significant risk factors for OIS. CONCLUSIONS: Patients with severe OCAD show hemodynamic changes that suggest reduced retrobulbar blood flow. Patients with severe bilateral OCAD, high-grade carotid stenosis, and reversed ophthalmic artery flow may have a greater risk of developing OIS.

Aged↗

Neomycin blocks dihydropyridine-insensitive Ca2+ influx in bovine adrenal chromaffin cells.

There is evidence that bovine adrenal chromaffin cells are provided with both dihydropyridine-sensitive and -resistant voltage-sensitive Ca2+ influx pathways. Although recent electrophysiological work indicates that the dihydropyridine-resistant pathway is partially mediated by omega-conotoxin-sensitive and -insensitive Ca2+ channels, the pharmacological sensitivity of the latter channels remains elusive. We have now found that combined incubations with nitrendipine (1 microM) and neomycin (0.5 mM) reduced high K+ (50 mM)-evoked intracellular Ca2+ concentration ([Ca2+]i) transients to a larger extent than each drug separately. [Ca2+]i was measured using the fluorescent intracellular Ca2+ indicator fura-2. Neomycin (0.05-2 mM) reduced high K(+)-evoked 45Ca2+ uptake in a dose-dependent manner (IC50 = 0.09 mM). In the presence of nitrendipine (1 microM), the minimal neomycin concentration necessary for total blockade of 45Ca2+ uptake was reduced to 0.3 mM. Moreover, in the absence of nitrendipine the 45Ca2+ uptake remaining in 0.3 mM neomycin (26% of maximum) was similar to the fractional inhibition by nitrendipine alone (29%). Neomycin (0.05-2 mM) inhibited the [Ca2+]i transient induced by the L-type Ca2+ channel agonist Bay K 8644 (1 microM) much more extensively at 2 mM than at 0.3 mM (percent inhibition = 59% and 15%, respectively). Neomycin (0.05-2 mM) blocked high K(+)-evoked noradrenaline and adrenaline release in a dose-dependent fashion (IC50 = 0.8-1.1 mM), the blockade efficiency being enhanced in the presence of 1 microM nitrendipine (IC50 = 0.17-0.19 mM). It is concluded that neomycin (< or = 0.3 mM) blocks preferentially the dihydropyridine-insensitive Ca2+ influx pathway of the chromaffin cell. Moreover, both the dihydropyridine-sensitive and the dihydropyridine-resistant, neomycin-sensitive Ca2+ influx pathways contribute strongly to depolarization-evoked catecholamine secretion.

Adrenal Medulla↗

Ins(1,4,5)P3 induces Ca2+ release from brain microsomes loaded either by the Ca2+ ATPase or by the Na+/Ca2+ exchanger.

In this study we investigated the release of Ca2+ in brain microsomes after Ca2+ loading by the Ca(2+)-ATPase or by the Na+/Ca2+ exchanger. The results show that in microsomes loaded with Ca2+ by the Ca(2+)-ATPase, Ins(1,4,5)P3 (5 microM) released 21 +/- 2% of the total Ca2+ accumulated, and that in the microsomes loaded with Ca2+ by the Na+/Ca2+ exchanger, Ins(1,4,5)P3 released 28 +/- 3% of the total Ca2+ accumulated. These results suggest that receptors of Ins(1,4,5)P3 may be co-localized with the Na+/Ca2+ exchanger in the endoplasmic reticulum membrane or that there are Ins(1,4,5)P3 receptors in the plasma membrane where the Na+/Ca2+ exchanger is normally present, or both. We also found that Ins(1,4,5)P3 inhibited the Ca(2+)-ATPase by 33.7%, but that it had no significant effect on the Na+/Ca2+ exchanger.

Animals↗

Synaptosomal [Ca2+]i as influenced by Na+/Ca2+ exchange and K+ depolarization.

The modulation of the intrasynaptosomal concentration of Ca2+, [Ca2+]i, by Na+/Ca2+ exchange was studied using Indo-1 fluorescence. The electrochemical gradient of Na+ was manipulated by substituting Li+ or choline for Na+ in the external medium and, then, the influx of 45Ca2+ and the [Ca2+]i were measured. It was found that the increase in [Ca2+]i induced by K+ depolarization is lower if the value of [Ca2+]i has been previously raised by Na+/Ca2+ exchange, suggesting that Ca2+ entering by Na+/Ca2+ exchange reduces the Ca2+ entering by voltage-dependent calcium channels. Our results show that a value of [Ca2+]i of about 650 nM induced by Na+/Ca2+ exchange reduces by 50% the Ca2+ entering due to K+ depolarization and no Ca2+ enters through the channels if the [Ca2+]i is previously raised above about 800 nM. Furthermore, predepolarization of the synaptosomes in a Ca-free medium also inhibits by at least 40% the [Ca2+]i rise through Ca2+ channels. Thus, the results suggest that both predepolarization and [Ca2+]i rise due to Na+/Ca2+ exchange decrease the Ca2+ entering by voltage-sensitive Ca2+ channels. The Ca2+ entering by Na+/Ca2+ exchange might contribute to the regulation of neurotransmitter release. Our results also show that the presence of Li+ in the external medium decreases the buffering capacity of synaptosomes, probably by releasing Ca2+ from mitochondria by Li+/Ca2+ exchange.

Animals↗

Influence of isolation media on synaptosomal properties: intracellular pH, pCa, and Ca2+ uptake.

Preparations of synaptosomes isolated in sucrose or in Na(+)-rich media were compared with respect to internal pH (pHi), internal Ca2+ concentration ([Ca2+]i), membrane potential and 45Ca2+ uptake due to K+ depolarization and Na+/Ca2+ exchange. We found that synaptosomes isolated in sucrose media have a pHi of 6.77 +/- 0.04 and a [Ca2+]i of about 260 nM, whereas synaptosomes isolated in Na(+)-rich ionic media have a pHi of 6.96 +/- 0.07 and a [Ca2+]i of 463 nM, but both types of preparations have similar membrane potentials of about -50 mV when placed in choline media. The sucrose preparation takes up Ca2+ only by voltage sensitive calcium channels (VSCC'S) when K(+)-depolarized, while the Na(+)-rich synaptosomes take up 45Ca2+ both by VSCC'S and by Na+/Ca2+ exchange. The amiloride derivative 2',4'-dimethylbenzamil (DMB), at 30 microM, inhibits both mechanisms of Ca2+ influx, but 5-(N-4-chlorobenzyl)-2',4' dimethylbenzamil (CBZ-DMB), at 30 microM, inhibits the Ca2+ uptake by VSCC'S, but not by Na+/Ca2+ exchange. Thus, DMB and CBZ-DMB permit distinguishing between Ca2+ flux through channels and through Na+/Ca2+ exchange. We point out that the different properties of the two types of synaptosomes studied account for some of the discrepancies in results reported in the literature for studies of Ca2+ fluxes and neurotransmitter release by different types of preparations of synaptosomes.

Amiloride↗

Partition coefficients of dopamine antagonists in brain membranes and liposomes.

Partition coefficients, Kp of dopamine antagonists, spiperone, haloperidol, domperidone and pimozide were determined in caudate nucleus microsomal membranes and in liposomes from membrane lipids. Kp values were measured as a function of temperature and the thermodynamics parameters for the transfer of the drugs from the aqueous medium to the lipid bilayer were evaluated. Partition in native membranes or in liposomes formed from the membrane lipids is not strongly dependent on temperature over the range from 8 to 37 degrees. The Kp values for spiperone, haloperidol and domperidone in membrane are 32 +/- 6, 192 +/- 11 and 308 +/- 40 respectively, whereas the equivalent values in liposomes are much higher: 195 +/- 12, 558 +/- 16 and 316 +/- 16. In contrast, for pimozide, the Kp values in membranes are higher than in liposomes: 1097 +/- 11 for microsomes and 662 +/- 10 for liposomes. Partition values in natural membranes decrease sequentially as follows: pimozide greater than domperidone greater than haloperidol greater than spiperone. Membranes rich in cholesterol show lower partition coefficients for haloperidol. The interaction of the antagonists with the bilayer is associated with small enthalpy changes and large increases in entropy, as expected for hydrophobic interactions. We conclude that the partition coefficients of the drugs studied for membranes and membranes lipids are very different from those reported for octanol/water and the latter values should not be used to estimate drug partition into membranes.

Animals↗

Effects of Ca2+ channel blockers on Ca2+ translocation across synaptosomal membranes.

The binding of [3H]nimodipine to purified synaptic plasma membranes (SPM) isolated from sheep brain cortex was characterized, and the effects of nimodipine, nifedipine, and (+)-verapamil on the [3H]nimodipine binding were compared to the effects on 45Ca2+ translocation under conditions that separate 45Ca2+ fluxes through Ca2+ channels from 45Ca2+ uptake via Na+/Ca2+ exchange. [3H]Nimodipine labels a single class of sites in SPM, with a KD of 0.64 +/- 0.1 nM, a Bmax of 161 +/- 27 fmol X mg-1 protein, and a Hill slope of 1.07, at 25 degrees C. Competition of [3H]nimodipine binding to purified SPM with unlabelled Ca2+ channel blockers shows that: nifedipine and nimodipine are potent competitors, with IC50 values of 4.7 nM and 5.9 nM, respectively; verapamil and (-)-D 600 are partial competitors, with biphasic competition behavior. Thus, (+)-verapamil shows an IC50 of 708 nM for the higher affinity component and the maximal inhibition is 50% of the specific binding, whereas for (-)-verapamil the IC50 is 120 nM, and the maximal inhibition is 30%; (-)-D 600 is even less potent than verapamil in inhibiting [3H]nimodipine binding (IC50 = 430 nM). However, (+)-verapamil, nifedipine, and nimodipine are less potent in inhibiting depolarization-induced 45Ca2+ influx into synaptosomes in the absence of Na+/Ca2+ exchange than in competing for [3H]nimodipine binding. Thus, (+)-verapamil inhibits Ca2+ influx by 50% at about 500 microM, whereas it inhibits 50% of the binding at concentrations 200-fold lower, and the discrepancy is even larger for the dihydropyridines. The Na+/Ca2+ exchange and the ATP-dependent Ca2+ uptake by SPM vesicles are also inhibited by the Ca2+ channel blockers verapamil, nifedipine, and d-cis-diltiazem, with similar IC50 values and in the same concentration range (10(-5)-10(-3) M) at which they inhibit Ca2+ influx through Ca2+ channels. We conclude that high-affinity binding of the Ca2+ blockers by SPM is not correlated with inhibition of the Ca2+ fluxes through channels in synaptosomes under conditions of minimal Na+/Ca2+ exchange. Furthermore, the relatively high concentrations of blockers required to block the channels also inhibit Ca2+ translocation through the Ca2+-ATPase and the Na+/Ca2+ exchanger. In this study, clear differentiation is made of the effects of the Ca2+ channel blockers on these three mechanisms of moving Ca2+ across the synaptosomal membrane, and particular care is taken to separate the contribution of the Na+/Ca2+ exchange from that of the Ca2+ channels under conditions of K+ depolarization.

Adenosine Triphosphatases↗

Calcium uptake related to K+-depolarization and Na+/Ca2+ exchange in sheep brain synaptosomes.

The uptake of Ca2+ by synaptosomes induced by K+-depolarization and by Na+/Ca2+ exchange was studied in synaptosomes in which the internal Na+ and K+ contents were varied by prolonged incubation at 30 degrees C or by inhibiting the Na+, K+-ATPase with 1 mM ouabain. Increased Na+ content of the synaptosomes is associated with an increase in Ca2+ uptake when the synaptosomes are placed in depolarizing K+ media. Furthermore, reduction in the [Na+]o, when the [K+]o is increased, in substitution for [Na+]o, to depolarize the membrane, further increases the Ca2+ uptake. Under these conditions, Ca2+ entry probably occurs through voltage-sensitive channels and through the Na+/Ca2+ exchanger. Destruction of the Na+ gradient by monensin, or preloading the synaptosomes with K+, completely inhibits the Ca2+ uptake in a K+-depolarizing medium. It is shown that if the Na+ gradient is maintained constant during K+-depolarization, the Ca2+ uptake is very low and that most of the Ca2+ uptake is correlated with the Na+ gradient. Evidence is presented that K+ may stimulate the Na+/Ca2+ exchange mechanism. Furthermore, divalent cations, Mg2+, Mn2+ and Zn2+, known to block Ca2+ channels, also inhibit Na+/Ca2+ exchange.

Animals↗

Effect of monovalent cations on Na+/Ca2+ exchange and ATP-dependent Ca2+ transport in synaptic plasma membranes.

Two Ca2+ transport systems were investigated in plasma membrane vesicles isolated from sheep brain cortex synaptosomes by hypotonic lysis and partial purification. Synaptic plasma membrane vesicles loaded with Na+ (Na+i) accumulate Ca2+ in exchange for Na+, provided that a Na+ gradient (in leads to out) is present. Agents that dissipate the Na+ gradient (monensin) prevent the Na+/Ca2+ exchange completely. Ca2+ accumulated by Na+/Ca2+ exchange can be released by A 23187, indicating that Ca2+ is accumulated intravesicularly. In the absence of any Na+ gradient (K+i-loaded vesicles), the membrane vesicles also accumulate Ca2+ owing to ATP hydrolysis. Monovalent cations stimulate Na+/Ca2+ exchange as well as the ATP-dependent Ca2+ uptake activity. Taking the value for Na+/Ca2+ exchange in the presence of choline chloride (external cation) as reference, other monovalent cations in the external media have the following effects: K+ or NH4+ stimulates Na+/Ca2+ exchange; Li+ or Cs+ inhibits Na+/Ca2+ exchange. The ATP-dependent Ca2+ transport system is stimulated by increasing K+ concentrations in the external medium (Km for K+ is 15 mM). Replacing K+ by Na+ in the external medium inhibits the ATP-dependent Ca2+ uptake, and this effect is due more to the reduction of K+ than to the elevation of Na+. The results suggest that synaptic membrane vesicles isolated from sheep brain cortex synaptosomes possess mechanisms for Na+/Ca2+ exchange and ATP-dependent Ca2+ uptake, whose activity may be regulated by monovalent cations, specifically K+, at physiological concentrations.

Adenosine Triphosphate↗